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Biochemistry 2 > ETC and Oxidative Phosphorylation > Flashcards

ETC and Oxidative Phosphorylation Flashcards

1
Q

what organelle produces ATP?

A

mitochondria

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2
Q

mitochondria anatomy

A

inner and outer membrane

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3
Q

where does oxidative phosphorylation occur?

A

inner mitochondrial membrane

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4
Q

what is oxidative phosphorylation (meaning of each word)?

A 
oxidation = molecules give up electrons
phosphorylation = addition of phosphate group to ADP to make ATP
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5
Q

oxidative phosphorylation overview sentence

A

make ATP by donating electrons to complexes in the inner mitochondrial membrane

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6
Q

what are the complexes?

A

proteins or lipids coupled with metals (EX: iron and copper)

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7
Q

what is the final electron acceptor

A

oxygen

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8
Q

overall purpose of oxidative phosphorylation?

A

create a proton gradient which is used to create ATP

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9
Q

What does ETC start with?

A

NADH and FADH2

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10
Q

where do we get NADH and FADH2 from?

A

1) glycolysis in cytoplasm
2) citric acid cycle in mitochondria
3) fatty acid oxidation in mitochondria

dehydrogenases help generate NADH and FADH2

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11
Q

how do NADH and FADH2 from cytoplasm (glycolysis) enter mitochondria for ETC?

A

the malate-aspartate shuttle (enter as NADH)

glycerol-3-phosphate shuttle (enter ETC at FADH2)

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12
Q

1st point of entry into ETC

A

Complex 1
contains flavin mononucleotide
and iron-sulfur centers (FeS)
NADH gives electron to NAD+

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13
Q

what can we do with NAD+ created by complex I

A

can be re-used by dehydrogenases to create more NADH

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14
Q

2nd point of entry into ETC

A

FADH2 donates electron to complex II and becomes FAD+

complex II = succinate dehydrogenase

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15
Q

relationship between CAC and ETC

A

they share a step! complex II (succinate dehydrogenase is also in CAC)
their activity rises and falls together

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16
Q

where do electrons from complex I and II go?

A

coenzyme Q (ubiquinone)

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17
Q

what is coenzyme Q

A

cholesterol derivative

it is the only lipid in the ETC

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18
Q

where does coenzyme Q send the electrons?

A

cytochromes! (Complex III)

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19
Q

what are cytochromes?

A

proteins with heme groups (contain iron)

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20
Q

heme group rxn

A

1) iron accepts an electron and goes from Fe3+ to Fe2+

2) iron releases electron to next cytochrome in chain and becomes Fe3+ again

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21
Q

complex III is made up of

A

cytochrome b and cytochrome c1

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22
Q

after complex III, electrons go to?

A

cytochrome c, then complex IV

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23
Q

complex IV is made up of?

A

cytochrome a and cytochrome a3 (together are called cytochrome oxidase)

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24
Q

what does cytochrome oxidase do?

A

transfer electrons to final electron acceptor (oxygen)

oxygen becomes electronegative enough to grab 2 protons and make water

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25
what happens in hypoxia (no oxygen)
ETC is interrupted, ATP synthesis doesn't happen
26
what does ETC produce?
the passing of electrons creates an electrical current which provides energy that allows protons to be pumped out of the mitochondria and into the space between the outer and inner mito membrane
27
which complexes span the inner mitochondrial membrane?
1, 3, and 4
28
how do complexes push protons?
as electrons move through, the complexes change conformation to push protons across
29
what do protons use to get across the mito membrane?
mito membrane is impermeable to protons | they use F0 proton channel attached to enzyme F1
30
what is F1
an ATP synthase that uses proton gradient to phosphorylate ADP into ATP sometimes called complex V
31
ADP/ATP antiport
pumps protons out of mitochondria and into cytoplasm | ATP leaves, a new ADP goes in to start cycle again
32
energy payoff for NADH
1 NADH makes 3 ATP | this is bc NADH activates 3 proton pumps (1, 3, and 4)
33
energy payoff for FADH2
1 FADH2 makes 2 ATP | bc it skips complex 1
34
those payoffs are called
P/O (phosphate: oxygen) ratios | bc they require oxygen as final electron acceptor
35
P/O ratio
rate of ATP produced per oxygen consumed for each molecule these are approximates
36
is ETC under hormonal control?
NO! | it is controlled by energy levels
37
high ATP
slow down ETC
38
high ADP
means low energy, speeds up ETC
39
drugs do what to OX phos
break it up via uncoupling or inhibition
40
uncoupling
ETC is normally coupled with ATP synthesis (they happen together) uncoupling agents break this link by inserting their own proton channels (ionophores) inter inner mitochondrial membrane or by carrying protons back into mito matrix
41
uncoupling agents cause bypass of what?
F0 (now F1 can't phosphorylate ADP into ATP) | they dissipate proton gradient
42
uncoupling agents where do electrons flow
electrons still flow up to oxygen red blood cells still deliver oxygen to tissues As ADP levels rise, body tries to make more NADH and FADH2 this is useless!
43
extra energy
we don't use electron's energy to move it across inner mito membrane, so more of that energy becomes heat energy
44
endogenous uncoupling agents
thermogenin
45
thermogenin
in brown adipose tissue of babies used to generate heat also found in hibernating animals aka uncoupling protein 1 (UCP1)
46
drug that is an uncoupling agent
``` high doses of aspirin leads to high metabolic rate causes metabolic acidosis if ATP gets too low, this leads to respiratory acidosis (combination is life threatening) ```
47
inhibition
chemicals/drugs inhibit components of ETC STOPS flow of electrons through ETC leads to decrease in ATP synthesis
48
what builds up during inhibition?
electron donors: NADH and FADH2 this means body will stop making more metabolic rate falls
49
poisons that inhibit ETC
lead to death quickly carbon monoxide, cyanide (inhibit complex IV) barbiturates (GABA agonists for seizure disorders) (inhibit complex I in high doses) oligomycin inhibits F0 component of ATP synthase
50
statins
decrease synthesis of coenzyme Q decreases ATP synthesis can lead to muscle pains and crams
51
mitochondria inner membrane...why is it folded?
to increase surface area for ETC!
52
as electrons go through chain, they
fall in energy and move toward progressively more positive reduction potentials
53
electron movement in Complex I
1) NADH binds Complex I 2) electrons move to FMN to Fe-S clusters 3) electrons reduce UQ to UQH2
54
MPP+
MPP+ inhibits complex I monoamine oxidase B (enzyme that creates MPP+) acts preferentially in cells of brain that produce dopamine (Parkinson's!)
55
Redox carriers in complex II
1) FAD picks up electrons from succinate | 2) electrons move through carriers until picked up by UQ
56
complex III overview
picks up electrons from UQH2 and gives them to cytochrome c (uses Q cycle)
57
electron carriers in complex III
cytochrome bL cytochrome bH cytochrome c1 Fe-S protein
58
cytochrome c
peripheral membrane protein that brings electrons to complex IV heme c is linked to it
59
Q cycle
in complex III | allows translocation of H+ across membrane as electrons are transferred between carriers
60
Q cycle net rxn
every 2 UQH2, 4 H+ cross membrane and 2 H+ regenerate UQH2
61
complex IV electron movement
in reduction of O2 to 2H2O (4 electrons): 4H+ used to reduce oxygen to water 4 H+ moved across membrane 8 H+ leave the matrix
62
chemiosmotic hypothesis
energy from electron transfer is stored in formation of proton gradient energy in proton gradient is coupled to ATP synthesis
63
F0 subunit
protons move through rotor (F0) which turns F1 subunit (the sphere)
64
C ring
Each subunit binds a proton to turn C ring | Fewer C subunits you have, fewer protons it takes for a 360 degree rotation
65
energy requiring step of ATP synthesis
ATP release from ATP synthase requires most energy | ATP synthesis itself doesn't require energy
66
flow of protons through ATP synthase
flow of protons through F0 subunit causes rotation of F- plus gamma. This rotation drives conformational changes in beta subunits that mediate binding of substrates, ATP synthesis, and release of ATP.
67
proton gradient requirements (2)
functional ETC and a proton-impermeable membrane
68
ETC and ATP synthesis inhibits
if one is inhibited, so is the other | EX: cyanide, azide, carbon monoxide, demerol, amytal
69
ATP-ADP translocase
moves ADP into mito matrix and ATP out of mito matrix
70
malate-aspartate shuttle
Malate to mitochondrial matrix Malate to oxaloacetate Oxaloacetate then leaves mitochondria as aspartate to reset the cycle In cytoplasm aspartate then becomes oxaloacetate again
71
glycerophosphate shuttle
transfers NADH in cytosol to mitochondria since inner mito membrane is impermeable to NADH and NAD+
72
Pasteur effect
Yeast metabolizing glucose, they use a lot more glucose under anaerobic than aerobic conditions (bc they still need to regenerate NAD+) BUT with no oxygen it's hard to regenerate NAD+ Anaerobic glycolysis = 2 ATP Aerobic glycolysis = 32-34 ATP Aerobic allows them to consume less glucose to get more energy

Biochemistry 2 (32 decks)

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